Arterial hypoxemia is a frequent and sometimes fatal complication of acute elevations of intracranial pressure. We propose to study the underlying neurogenic mechanism responsible for this phenomenon in the hope that this information will lead to the early detection and reversal of this malfunction as well as provide some insight into the mechanisms responsible for the homeostatic matching of pulmonary perfusion and ventilation in the normal lung. Personal observations in patients with acute elevations of intracranial pressure suggest (a) that this phenomenon occurs most consistently in decerebrate patients, and (b) that the hypoxemia is secondary to a mismatching of pulmonary ventilation and perfusion (VA/Q). Acute increased intracranial pressure will be produced in experimental animals by the inflation of epidural balloons with simultaneous monitoring of arterial blood gases by means of a mass spectrometer. This allows for the immediate observation of arterial hypoxemia. Measurements (a-A)DN2 will disclose the development of a maldistribution of VA/Q. Subsequent investigations will be done to determine if this maldistribution of VA/Q is due primarily to a disturbance in perfusion or is related to a disturbance in ventilation. The underlying neurogenic reflex mechanisms responsible for this phenomenon will be investigated by the use of pharmacological blocking agents.